Metoclopramide inhibits proliferation of leukemia stem cells, finds study
Chronic myeloid leukemia (CML) results from a degeneration of the hematopoietic stem cells (leukemia stem cells), thereby leading to the uncontrolled formation of specific white blood cells, the so-called granulocytes. Research work at the Department of Medical Oncology at the Inselspital, Bern University Hospital and the University of Bern focused therefore on identifying the signaling pathways and control mechanisms of the leukemia stem cell. A promising approach is provided by working with MPR, an anti-emetic medication commonly used to treat nausea and vomiting.
Specific blocking of leukemia stem cell proliferation with metoclopramide
The exact role of the surface molecule CD93 (cluster of differentiation 93) in controlling the proliferation of leukemia stem cells was analyzed and documented, initially in animal experiments and subsequently in experiments with leukemia stem cells from patients. This revealed a distinct regulatory function of CD93 in leukemia stem cells. To begin with, the effect was demonstrated in vivo in animal experiments. It was further shown that the control function only applies to leukemia stem cells, not to normal hematopoietic stem cells. Furthermore, it was demonstrated that the anti-emetic MPR interrupts the signaling pathway that stimulates cell proliferation of leukemia stem cells in vitro and also, in animal experiments, visibly improves survival with CML by blocking the proliferation of leukemia stem cells. This provides strong evidence that MPR may also show positive results in treating CML in humans.
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